Lesões crônicas em camundongos deficientes no receptor 1 do TNF infectados com Leishmania braziliensis: desenvolvimento de um modelo para estudo da leishmaniose mucocutânea

• Ano de defesa: 2015
• Autor(a) principal: Paula Seixas Mello
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; UFMG
• Palavras-chave em Português: Leishmania braziliensis; Leishmaniose; Muco-cutânea; TNFR1; Bioquímica e imunologia
• Link de acesso: http://hdl.handle.net/1843/BUBD-A3REUY

Leishmaniasis is the name given to the disease caused by protozoa parasites of the genus Leishmania. Depending on the species a broad spectrum of clinical manifestations can be observed both locally and systemically during the infection. Leishmaniasis constitute an important public health problem worldwide, especially in developing countries, for example, Brazil. Mucocutaneous leishmaniasis is characterized by the development of chronic lesions disseminated to the oral and the nasal mucosa of patients, but with low parasite load. There is no specific murine model that mimics all the immunopathological characteristics described in humans. However, our group has recently shown that TNFR1 KO mouse infected with L. major can present some features that correlate with symptoms described in humans. The aim of this study was to evaluate the infection of TNFR1 KO mice by L. braziliensis attempting to develop an experimental model for mucocutaneous leishmaniasis. Our observations indicate similarities in the inflammatory infiltrate between human and TNFR1 KO mice lesions. There was an increase in TCD8+ lymphocytes and neutrophils in the site of infection that remain even after controlling the parasitism. Infiltration of these cells promote intense release of pro-inflammatory cytokines such as TNF and IFN-. Similar levels of IL-10 from C57BL/6 (wild-type) and TNFR1 KO mice suggest that the lack of regulation of the inflammatory process in these animals can be one of the factors that promote the spreading of parasites and maintenance of inflammatory cells in the lymph nodes and spleen during the advanced stages of the disease. Nevertheless, we did not detect the presence of mucosal lesions in those mice, suggesting that the manifestation of the disease is the result of the interaction of multiple factors inherent not only to the parasite, but also the host.